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DUFOUR (CC BY-NC-ND 2.0)

UNIVERSITE CLAUDE BERNARD – LYON 1

FACULTE DE MEDECINE LYON EST

Année 2015 N°

TRAITEMENT ENDOVASCULAIRE DES PATHOLOGIES AIGUES ET CHRONIQUES DE L’AORTE

THORACIQUE : EVALUATION APRES 6 ANS DE SURVEILLANCE

THESE

Présentée

A l’Université Claude Bernard Lyon 1

et soutenue publiquement le 26 Mai 2015

pour obtenir le grade de Docteur en Médecine

par

Clémence DUFOUR

Née le 22 septembre 1986 à Lyon


UNIVERSITE CLAUDE BERNARD – LYON 1 ___________________

. Président de l'Université François-Noël GILLY . Président du Comité de Coordination François-Noël GILLY des Etudes Médicales

. Secrétaire Général Alain HELLEU

SECTEUR SANTE

UFR DE MEDECINE LYON EST Doyen : Jérôme ETIENNE

UFR DE MEDECINE

LYON SUD – CHARLES MERIEUX Doyen : Carole BURILLON

INSTITUT DES SCIENCES PHARMACEUTIQUES ET BIOLOGIQUES (ISPB) Directrice: Christine VINCIGUERRA

UFR D'ODONTOLOGIE Directeur : Denis BOURGEOIS

INSTITUT DES SCIENCES ET TECHNIQUES DE READAPTATION Directeur : Yves MATILLON DEPARTEMENT DE FORMATION ET CENTRE DE RECHERCHE EN BIOLOGIE HUMAINE Directeur : Pierre FARGE

SECTEUR SCIENCES ET TECHNOLOGIES

UFR DE SCIENCES ET TECHNOLOGIES Directeur : Fabien de MARCHI

UFR DE SCIENCES ET TECHNIQUES DES ACTIVITES PHYSIQUES ET SPORTIVES (STAPS) Directeur : Claude COLLIGNON

POLYTECH LYON Directeur : Pascal FOURNIER

I.U.T. Directeur : Christian COULET

INSTITUT DES SCIENCES FINANCIERES ET ASSURANCES (ISFA) Directeur : Véronique MAUME-DESCHAMPS I.U.F.M. Directeur : Régis BERNARD

CPE Directeur : Gérard PIGNAULT


Faculté de Médecine Lyon Est Liste des enseignants 2014/2015

Professeurs des Universités – Praticiens Hospitaliers Classe exceptionnelle Echelon 2 Cochat Pierre Pédiatrie Cordier Jean-François Pneumologie ; addictologie Etienne Jérôme Bactériologie-virologie ; hygiène hospitalière Gouillat Christian Chirurgie digestive Guérin Jean-François Biologie et médecine du développement

et de la reproduction ; gynécologie médicale Mauguière François Neurologie Ninet Jacques Médecine interne ; gériatrie et biologie du vieillissement ; médecine générale ; addictologie Peyramond Dominique Maladie infectieuses ; maladies tropicales Philip Thierry Cancérologie ; radiothérapie Raudrant Daniel Gynécologie-obstétrique ; gynécologie médicale Rudigoz René-Charles Gynécologie-obstétrique ; gynécologie médicale Professeurs des Universités – Praticiens Hospitaliers Classe exceptionnelle Echelon 1 Baverel Gabriel Physiologie Blay Jean-Yves Cancérologie ; radiothérapie Borson-Chazot Françoise Endocrinologie, diabète et maladies métaboliques ; gynécologie médicale Denis Philippe Ophtalmologie Finet Gérard Cardiologie Guérin Claude Réanimation ; médecine d’urgence Lehot Jean-Jacques Anesthésiologie-réanimation ; médecine d’urgence Lermusiaux Patrick Chirurgie thoracique et cardiovasculaire Martin Xavier Urologie Mellier Georges Gynécologie-obstétrique ; gynécologie médicale Michallet Mauricette Hématologie ; transfusion Miossec Pierre Immunologie Morel Yves Biochimie et biologie moléculaire Mornex Jean-François Pneumologie ; addictologie Neyret Philippe Chirurgie orthopédique et traumatologique Ninet Jean Chirurgie thoracique et cardiovasculaire Ovize Michel Physiologie Ponchon Thierry Gastroentérologie ; hépatologie ; addictologie Pugeat Michel Endocrinologie, diabète et maladies métaboliques ; gynécologie médicale Revel Didier Radiologie et imagerie médicale Rivoire Michel Cancérologie ; radiothérapie Thivolet-Bejui Françoise Anatomie et cytologie pathologiques Vandenesch François Bactériologie-virologie ; hygiène hospitalière Zoulim Fabien Gastroentérologie ; hépatologie ; addictologie


Professeurs des Universités – Praticiens Hospitaliers Première classe André-Fouet Xavier Cardiologie Barth Xavier Chirurgie générale Berthezene Yves Radiologie et imagerie médicale Bertrand Yves Pédiatrie Beziat Jean-Luc Chirurgie maxillo-faciale et stomatologie Boillot Olivier Chirurgie digestive Braye Fabienne Chirurgie plastique, reconstructrice et esthétique ; brûlologie Breton Pierre Chirurgie maxillo-faciale et stomatologie Chassard Dominique Anesthésiologie-réanimation ; médecine d’urgence Chevalier Philippe Cardiologie Claris Olivier Pédiatrie Colin Cyrille Epidémiologie, économie de la santé et prévention Colombel Marc Urologie Cottin Vincent Pneumologie ; addictologie D’Amato Thierry Psychiatrie d’adultes ; addictologie Delahaye François Cardiologie Di Fillipo Sylvie Cardiologie Disant François Oto-rhino-laryngologie Douek Philippe Radiologie et imagerie médicale Ducerf Christian Chirurgie digestive Dumontet Charles Hématologie ; transfusion Durieu Isabelle Médecine interne ; gériatrie et biologie du vieillissement ; médecine générale ; addictologie Edery Charles Patrick Génétique Fauvel Jean-Pierre Thérapeutique ; médecine d’urgence ; addictologie

Gaucherand Pascal Gynécologie-obstétrique ; gynécologie médicale Guenot Marc Neurochirurgie Gueyffier François Pharmacologie fondamentale ; pharmacologie clinique ; addictologie Guibaud Laurent Radiologie et imagerie médicale Herzberg Guillaume Chirurgie orthopédique et traumatologique Honnorat Jérôme Neurologie Lachaux Alain Pédiatrie Lina Bruno Bactériologie-virologie ; hygiène hospitalière Lina Gérard Bactériologie-virologie ; hygiène hospitalière Mabrut Jean-Yves Chirurgie générale Mertens Patrick Anatomie Mion François Physiologie Morelon Emmanuel Néphrologie Moulin Philippe Nutrition Négrier Claude Hématologie ; transfusion Négrier Marie-Sylvie Cancérologie ; radiothérapie Nicolino Marc Pédiatrie Nighoghossian Norbert Neurologie Obadia Jean-François Chirurgie thoracique et cardiovasculaire Picot Stéphane Parasitologie et mycologie Rode Gilles Médecine physique et de réadaptation Rousson Robert-Marc Biochimie et biologie moléculaire Roy Pascal Biostatistiques, informatique médicale et technologies de communication Ruffion Alain Urologie Ryvlin Philippe Neurologie Scheiber Christian Biophysique et médecine nucléaire


Schott-Pethelaz Anne-Marie Epidémiologie, économie de la santé et prévention Terra Jean-Louis Psychiatrie d’adultes ; addictologie Tilikete Caroline Physiologie Touraine Jean-Louis Néphrologie Truy Eric Oto-rhino-laryngologie Turjman Francis Radiologie et imagerie médicale Vallée Bernard Anatomie Vanhems Philippe Epidémiologie, économie de la santé et prévention Professeurs des Universités – Praticiens Hospitaliers Seconde Classe Allaouchiche Bernard Anesthésiologie-réanimation ; médecine d’urgence Argaud Laurent Réanimation ; médecine d’urgence Aubrun Frédéric Anesthésiologie-réanimation ; médecine d’urgence Badet Lionel Urologie Bessereau Jean-Louis Biologie cellulaire Boussel Loïc Radiologie et imagerie médicale Calender Alain Génétique Charbotel Barbara Médecine et santé au travail Chapurlat Roland Rhumatologie Cotton François Radiologie et imagerie médicale Dalle Stéphane Dermato-vénéréologie Dargaud Yesim Hématologie ; transfusion Devouassoux Mojgan Anatomie et cytologie pathologiques Dubernard Gil Gynécologie-obstétrique ; gynécologie médicale Dumortier Jérome Gastroentérologie ; hépatologie ; addictologie Fanton Laurent Médecine légale Faure Michel Dermato-vénéréologie Fellahi Jean-Luc Anesthésiologie-réanimation ; médecine d’urgence Ferry Tristan Maladie infectieuses ; maladies tropicales Fourneret Pierre Pédopsychiatrie ; addictologie Gillet Yves Pédiatrie Girard Nicolas Pneumologie Gleizal Arnaud Chirurgie maxillo-faciale et stomatologie Guyen Olivier Chirurgie orthopédique et traumatologique Henaine Roland Chirurgie thoracique et cardiovasculaire Hot Arnaud Médecine interne Huissoud Cyril Gynécologie-obstétrique ; gynécologie médicale

Jacquin-Courtois Sophie Médecine physique et de réadaptation

Janier Marc Biophysique et médecine nucléaire Javouhey Etienne Pédiatrie Juillard Laurent Néphrologie Jullien Denis Dermato-vénéréologie Kodjikian Laurent Ophtalmologie Krolak Salmon Pierre Médecine interne ; gériatrie et biologie du vieillissement ; médecine générale ; addictologie Lejeune Hervé Biologie et médecine du développement et de la reproduction ; gynécologie médicale Merle Philippe Gastroentérologie ; hépatologie ; addictologie Michel Philippe Epidémiologie, économie de la santé et prévention Monneuse Olivier Chirurgie générale Mure Pierre-Yves Chirurgie infantile Nataf Serge Cytologie et histologie Pignat Jean-Christian Oto-rhino-laryngologie Poncet Gilles Chirurgie générale


Raverot Gérald Endocrinologie, diabète et maladies métaboliques ; gynécologie médicale Ray-Coquard Isabelle Cancérologie ; radiothérapie Richard Jean-Christophe Réanimation ; médecine d’urgence Rossetti Yves Physiologie Rouvière Olivier Radiologie et imagerie médicale Saoud Mohamed Psychiatrie d’adultes Schaeffer Laurent Biologie cellulaire Souquet Jean-Christophe Gastroentérologie ; hépatologie ; addictologie Vukusic Sandra Neurologie Wattel Eric Hématologie ; transfusion Professeur des Universités - Médecine Générale Letrilliart Laurent Moreau Alain Professeurs associés de Médecine Générale Flori Marie Lainé Xavier Zerbib Yves Professeurs émérites Chatelain Pierre Pédiatrie Bérard Jérôme Chirurgie infantile Boulanger Pierre Bactériologie-virologie ; hygiène hospitalière Bozio André Cardiologie Chayvialle Jean-Alain Gastroentérologie ; hépatologie ; addictologie Daligand Liliane Médecine légale et droit de la santé Descotes Jacques Pharmacologie fondamentale ; pharmacologie Droz Jean-Pierre Cancérologie ; radiothérapie Floret Daniel Pédiatrie Gharib Claude Physiologie Itti Roland Biophysique et médecine nucléaire Kopp Nicolas Anatomie et cytologie pathologiques Neidhardt Jean-Pierre Anatomie Petit Paul Anesthésiologie-réanimation ; médecine d’urgence Rousset Bernard Biologie cellulaire Sindou Marc Neurochirurgie Trepo Christian Gastroentérologie ; hépatologie ; addictologie Trouillas Paul Neurologie Trouillas Jacqueline Cytologie et histologie Viale Jean-Paul Réanimation ; médecine d’urgence Maîtres de Conférence – Praticiens Hospitaliers Hors classe Benchaib Mehdi Biologie et médecine du développement et de la reproduction ; gynécologie médicale


Bringuier Pierre-Paul Cytologie et histologie Davezies Philippe Médecine et santé au travail Germain Michèle Physiologie Jarraud Sophie Bactériologie-virologie ; hygiène hospitalière Jouvet Anne Anatomie et cytologie pathologiques Le Bars Didier Biophysique et médecine nucléaire Normand Jean-Claude Médecine et santé au travail Persat Florence Parasitologie et mycologie Pharaboz-Joly Marie-Odile Biochimie et biologie moléculaire Piaton Eric Cytologie et histologie Rigal Dominique Hématologie ; transfusion Sappey-Marinier Dominique Biophysique et médecine nucléaire Streichenberger Nathalie Anatomie et cytologie pathologiques Timour-Chah Quadiri Pharmacologie fondamentale ; pharmacologie clinique ; addictologie Voiglio Eric Anatomie Wallon Martine Parasitologie et mycologie Maîtres de Conférence – Praticiens Hospitaliers Première classe Ader Florence Maladies infectieuses ; maladies tropicales Barnoud Raphaëlle Anatomie et cytologie pathologiques Bontemps Laurence Biophysique et médecine nucléaire Chalabreysse Lara Anatomie et cytologie pathologiques Charrière Sybil Nutrition Collardeau Frachon Sophie Anatomie et cytologie pathologiques Cozon Grégoire Immunologie Dubourg Laurence Physiologie Escuret Vanessa Bactériologie-virologie ; hygiène hospitalière Hervieu Valérie Anatomie et cytologie pathologiques Kolopp-Sarda Marie Nathalie Immunologie Laurent Frédéric Bactériologie-virologie ; hygiène hospitalière Lesca Gaëtan Génétique Maucort Boulch Delphine Biostatistiques, informatique médicale et technologies de communication Meyronet David Anatomie et cytologie pathologiques Peretti Noel Nutrition Pina-Jomir Géraldine Biophysique et médecine nucléaire Plotton Ingrid Biochimie et biologie moléculaire Rabilloud Muriel Biostatistiques, informatique médicale et technologies de communication Ritter Jacques Epidémiologie, économie de la santé et prévention Roman Sabine Physiologie Tardy Guidollet Véronique Biochimie et biologie moléculaire Tristan Anne Bactériologie-virologie ; hygiène hospitalière Vlaeminck-Guillem Virginie Biochimie et biologie moléculaire Maîtres de Conférences – Praticiens Hospitaliers Seconde classe Casalegno Jean-Sébastien Bactériologie-virologie ; hygiène hospitalière


Chêne Gautier Gynécologie-obstétrique ; gynécologie médicale Duclos Antoine Epidémiologie, économie de la santé et prévention Phan Alice Dermato-vénéréologie Rheims Sylvain Neurologie Rimmele Thomas Anesthésiologie-réanimation ; médecine d’urgence Schluth-Bolard Caroline Génétique Simonet Thomas Biologie cellulaire Thibault Hélène Physiologie Vasiljevic Alexandre Anatomie et cytologie pathologiques Venet Fabienne Immunologie Maîtres de Conférences associés de Médecine Générale Chanelière Marc Farge Thierry Figon Sophie


Le Serment d'Hippocrate

Je promets et je jure d'être fidèle aux lois de l’honneur et de la probité dans l'exercice de la

Médecine.

Je respecterai toutes les personnes, leur autonomie et leur volonté, sans discrimination.

J'interviendrai pour les protéger si elles sont vulnérables ou menacées dans leur intégrité ou

leur dignité. Même sous la contrainte, je ne ferai pas usage de mes connaissances contre les lois

de l'humanité.

J'informerai les patients des décisions envisagées, de leurs raisons et de leurs

conséquences. Je ne tromperai jamais leur confiance.

Je donnerai mes soins à l'indigent et je n'exigerai pas un salaire au dessus de mon travail.

Admis dans l'intimité des personnes, je tairai les secrets qui me seront confiés et ma

conduite ne servira pas à corrompre les mœurs.

Je ferai tout pour soulager les souffrances. Je ne prolongerai pas abusivement la vie ni ne

provoquerai délibérément la mort.

Je préserverai l'indépendance nécessaire et je n'entreprendrai rien qui dépasse mes

compétences. Je perfectionnerai mes connaissances pour assurer au mieux ma mission.

Que les hommes m'accordent leur estime si je suis fidèle à mes promesses. Que je sois

couvert d'opprobre et méprisé si j'y manque.


COMPOSITION DU JURY

PRESIDENT

Monsieur le Professeur Philippe DOUEK

MEMBRES

Monsieur le Professeur Didier REVEL

Monsieur le Professeur Jean-Pierre PRACROS

Monsieur le Professeur Laurent GUIBAUD

Monsieur le Professeur Loïc BOUSSEL

Monsieur le Docteur Jacques ROBIN


REMERCIEMENTS

A mon président du jury et directeur de thèse, Monsieur le Professeur Philippe Douek,

Je vous remercie d’avoir dirigé et accompagné ce travail de thèse, et de me faire l’honneur de

présider ce jury. Votre expérience clinique et votre rigueur scientifique m’ont été précieuses pour

l’élaboration de ce travail, de même que la pertinence de vos remarques qui m’ont aidée à

approfondir ma réflexion. Vous m’avez aussi appris à persévérer et encouragée lors de la

publication de notre article, je vous en remercie.

Veuillez trouver ici le témoignage de ma plus grande estime et de ma sincère reconnaissance.

A Monsieur le Professeur Didier Revel, C’est un grand honneur de pouvoir vous compter parmi mon jury de thèse. Vos qualités professionnelles et votre rigueur sont pour moi des exemples à suivre. J’ai été marquée par votre implication pour l’encadrement des internes et votre bienveillance constante. Mon stage passé à vos côtés a été l’un des plus formateurs. Soyez assuré de mon plus grand respect et de ma considération.

A Monsieur le Professeur Loïc Boussel, Je te remercie d’avoir accepté d’être membre de mon jury et pour toute l’aide apportée pour ce travail de thèse. Merci pour ta disponibilité, tes conseils pertinents et ton enthousiasme contagieux pour les travaux scientifiques. Sois assuré de ma plus grande gratitude et de tout mon respect.

A Monsieur le Professeur Jean-Pierre Pracros, C’est un grand honneur de pouvoir vous compter parmi mon jury de thèse. Depuis mon passage dans votre service, je souhaite rejoindre votre équipe et partager votre passion pour cette merveilleuse spécialité. J’ai été marquée par votre disponibilité, votre implication et votre générosité dans le partage des connaissances, et ce toujours dans la bonne humeur. Je suis impatiente de bientôt venir travailler à vos côtés. Soyez assuré de ma plus grande estime et de ma sincère admiration.

A Monsieur le Professeur Laurent Guibaud,

Je te remercie d’avoir accepté de participer à mon jury de thèse. Au-delà de tes compétences médicales, ta disponibilité et ton implication dans notre futur à l’HFME m’ont beaucoup touchée. J’espère ne pas te décevoir dans mon futur travail, et serai très heureuse de travailler à tes côtés. Sois assuré de ma plus grande estime et de toute ma gratitude.

A Monsieur le Docteur Jacques Robin,

Je vous suis très reconnaissante d’avoir accepté de juger ce travail. Votre expérience clinique et chirurgicale apportera un éclairage pragmatique à cette étude.

Soyez assuré de ma sincère considération.


A l’ensemble des Maîtres qui ont contribué à ma formation et à mon intérêt pour la radiologie :

Monsieur le Professeur Yves Berthezène

Monsieur le Professeur Loïc Boussel

Monsieur le Professeur Jean-Pierre Pracros

Monsieur le Professeur Laurent Guibaud

Monsieur le Professeur Olivier Rouvière

Monsieur le Professeur Didier Revel

Monsieur le Professeur Philippe Douek

Monsieur le Professeur Pierre-Jean Valette

Monsieur le Professeur Jean-Baptiste Pialat

A Delphine Gamondes : Un grand merci pour ton aide et ton soutien pour ce travail. J’ai énormément apprécié travailler avec toi : compétente, dynamique, organisée et toujours de bonne humeur, tu es un modèle pour moi !

A l’ensemble des praticiens hospitaliers, assistants et chefs de clinique pour leur pédagogie, leurs compétences et disponibilité :

A Croix-Rousse, merci à vous tous qui m’avez initiée à la radiologie : A. Rode, M. Durieux, A. Coulon, E. Maissiat, H. Saint-Laurent, C. Journe, V. Thomson, J. Vicente, AF. Manichon, JF. Bergerot

A toute l’équipe de l’HFME, que je rejoindrai avec plaisir : J. Payen De La Garanderie, S. Lorthois-Ninou, I. Canterino, C.Rannou-Haverlant, L. Viremouneix, M. Cagneaux, B. Morel, M. Gignier

A HEH : S. Arion, G. Pagnoux, M. Papillard, M. Tigel, C. Mastier, C. Amanieu, A. Muller, JR. Risson, A. Ltaief-Boudrigua, A. Martinon, L. Manera

A Cardio : Sophie Gonidec

A Neuro, qui restera un de mes meilleurs souvenirs de stage avec L. Chamard, G. Louis-Tisserand, M. Hermier, A. Geraldo da Silva Couceiro, A. Basle

A tous mes cointernes :

Jean-Christophe, Tatiana, Marc, Isabelle, Leila, Roxana, Rihad, Thomas, Flavie, Charlotte, Kheang, Paul-Henri, Johan, Elodie, Audrey Lacalm, Lidy, Audrey Haquin, Alexandre, Laura-Anne et la neuro-team : Clément, Audrey et Laurène

Et à tous ceux que je n’aurais pas eu la chance d’avoir comme cointernes.

Aux amis d’internat : Raphi, JT, Benou, Fabien, Virginie, Elodie (merci pour tous les debriefs passés et tous ceux à venir !), et ma future co-chef Audrey

Aux pédiatres : Monsieur le Professeur Bellon, Monsieur le Professeur Reix, C. Chanelière, S. Vrielynck, et mes co-internes Laurène et Lélia.

Aux manips de G, HFME, Lyon Sud, Croix-Rousse et neuro : pour toutes ces journées et longues nuits de gardes passées à vos côtés.

A tous les manipulateurs, pour votre investissement, votre gentillesse et votre bonne humeur !

Aux secrétaires qui nous facilitent la vie au quotidien. Une mention particulière à Delphine et Véronique pour votre disponibilité et votre accueil toujours chaleureux.


A mes amies de toujours Sabine et Raphie : même si l’on se voit moins souvent, même si l’on est plus loin, même si on a aujourd’hui chacune nos vies, c’est toujours un bonheur de vous retrouver ! Je serai toujours là pour vous !

A ma petite filleule Emma, que je ne vois pas assez souvent, mais qui m’émerveille à chaque fois

A ma famille

A Thomas, mon chéri, Avec toi je suis tout simplement heureuse. Je suis fière de toi, de nous, de la famille que nous construisons et qui je l’espère s’agrandira encore. Merci pour ton soutien quotidien pour tout ce que j’entreprends, tu sais me faire rire et toujours trouver les mots justes pour me rassurer et me redonner le moral. Merci pour ton aide très précieuse tout au long de ce travail surtout en informatique (ça ne marche jamais comme je veux, ce n’est pas de ma faute), en anglais et en orthographe ;-) Merci pour ta patience lors des multiples relectures et corrections. Je t’aime.

A Antoine, mon petit chéri,

Te voir grandir et progresser nous émerveille au quotidien. Tu as déjà ton caractère mais aussi plein d’humour ! Très bon public et joueur, tu nous remplis de bonheur ! Tout ce qui m’importe est que tu sois heureux. Je t’aime.

A mes parents, Je ne sais comment vous exprimer ma reconnaissance pour votre soutien sans faille tout au long de ces années d’étude, surtout dans les moments difficiles. Merci pour votre positivisme, qui m’aide à relativiser et avancer, merci pour votre aide et tout l’amour que vous nous donnez. Sans vous je ne serai pas ce que je suis aujourd’hui. Je ne trouve pas de mot assez fort pour vous l’exprimer : un grand merci !

A mes frères et sœurs : JB, Méla, Gus et Delph, merci pour m’avoir soutenue (et supportée !!) pendant toutes ces années d’études, merci pour votre humour et chamailleries qu’on aime toujours autant quand on se retrouve et qui je l’espère ne changeront jamais !

A mes beaux-frères et belles-sœurs qui viennent agrandir et enrichir la famille !

A mes neveux adorés : Louis, Arthur, Lucas et tous les futurs !

A ma belle-famille : Dominique, Christian, Max et Axelle, merci pour votre accueil toujours parfait, les bons repas du dimanche (surtout les mousses au chocolat !) et toutes les soirées jeux (où je n’aime toujours pas perdre !) Je me suis toujours sentie la bienvenue dans ma deuxième famille. Vous comptez énormément pour moi.

A Grand-Père, Mamé, ma marraine Marie-Do, mes oncles et tantes, cousins et cousines : les retrouvailles se font plus rares, mais je les apprécie toujours autant !

Une mention spéciale pour Anne qui m’a initiée aux statistiques,

et pour Noémie pour l’assistance téléphonique excel !


TRAITEMENT ENDOVASCULAIRE DES PATHOLOGIES

AIGÜES ET CHRONIQUES DE L’AORTE THORACIQUE :

EVALUATION APRES 6 ANS DE SURVEILLANCE


1

TABLE DES MATIÈRES

PRÉAMBULE ............................................................................................................................. 2

RÉSUMÉ (en français) ................................................................................................................ 7

ABSTRACT .................................................................................................................................. 9

1. INTRODUCTION ................................................................................................................. 11

2. MATERIAL AND METHODS ............................................................................................. 12

2.1. Endovascular procedure .................................................................................................. 12

2.2. Clinical follow-up ........................................................................................................... 13

2.3. Imaging evaluation ......................................................................................................... 14

2.4. Statistical analysis ........................................................................................................... 14

3. RESULTS .............................................................................................................................. 16

3.1. Perioperative mortality and adverse events .................................................................... 17

3.2. Long-term mortality and adverse events ........................................................................ 17

3.3. Thoracic aortic aneurysms .............................................................................................. 24

3.4. Thoracic dissections ........................................................................................................ 25

3.5. Traumatic aortic injuries ................................................................................................. 28

3.6. Pseudo-aneurysms and penetrating ulcer ........................................................................ 29

4. DISCUSSION ....................................................................................................................... 30

4.1. Thoracic aortic aneurysms .............................................................................................. 30

4.2. Thoracic dissections ........................................................................................................ 32

4.3. Traumatic aortic injuries ................................................................................................. 34

4.4. Pseudo-aneurysms and penetrating ulcer ........................................................................ 35

4.5. Limitations ...................................................................................................................... 35

REFERENCES ............................................................................................................................ 36

ARTICLE ORIGINAL: “Pathology-specific late outcome after endovascular repair of the

thoracic aorta: a single-center experience.”

CONCLUSION


2

PREAMBULE

Le traitement endovasculaire de l’aorte thoracique est devenu une alternative peu invasive

à la chirurgie de remplacement aortique pour le traitement des pathologies de l’aorte thoracique

telles que les ruptures de l’isthme aortique, les dissections aortiques de type B, les anévrismes de

l’aorte thoracique descendante ou les ulcères aortiques pénétrants.

Le concept d’endoprothèse aortique a vu le jour en 1991, proposé par Parodi et al. (1)

pour le traitement de lésions anévrismales de l’aorte sous-rénale. Peu de temps plus tard, Dake et

al. (2) reprirent ce concept et le développèrent en élargissant ses indications au traitement des

anévrismes de l’aorte thoracique descendante et aux dissections de type B de l’aorte thoracique.

A Lyon, la première implantation d’endoprothèse aortique thoracique a eu lieu en 1999,

pour le traitement d’un patient présentant un faux anévrisme de l’isthme aortique, sans

complication péri-opératoire ou à distance après un suivi de plus de 15 ans.

Rapidement convaincus du bien-fondé de cette nouvelle technique, les indications

d’endoprothèse aortique thoracique se sont peu à peu étendues chez des patients rigoureusement

sélectionnés, en alternative à la chirurgie de remplacement de l’aorte thoracique sous circulation

extracorporelle, encore grevée d’une morbi-mortalité péri-opératoire non négligeable.

Une base de données patients a alors été mise en place pour recueillir l’ensemble des

données cliniques et paracliniques, incluant les angio-scanner et angio-IRM initiaux et réalisés

lors du suivi des patients présentant des lésions de l’aorte thoracique traitées par endoprothèse.

Une première étude sur l’évaluation à court terme du traitement endovasculaire des

lésions de l’aorte thoracique a été publiée en 2007, à partir de la cohorte de notre base de

données, avec un suivi moyen de 15 mois après traitement (3). En accord avec d’autres travaux


3

(4–6), cette étude a démontré la faisabilité et l’efficacité du traitement endovasculaire de diverses

lésions de l’aorte thoracique (anévrismes, dissections de type B, pseudo-anévrismes, rupture de

l’isthme, ulcères pénétrants), sans élévation de la morbi-mortalité par rapport au traitement

chirurgical de référence (remplacement aortique).

En effet, en dépit des progrès des techniques chirurgicales et de réanimation, le

remplacement chirurgical de l’aorte thoracique descendante est encore associé à un taux élevé de

mortalité (5.7% à 15.1%) (7), en particulier pour les patients âgés, traités en urgence ou à haut

risque chirurgical.

Le traitement endovasculaire de l’aorte thoracique offre donc une alternative prometteuse,

d’autant plus que la plupart des études s’accordent à montrer une réduction des taux de morbidité

et de mortalité péri-opératoire comparativement à la chirurgie conventionnelle (4,8).

Cependant, la sélection rigoureuse des patients est une condition indispensable au succès

du traitement endovasculaire des pathologies de l’aorte thoracique descendante. Cette étape

cruciale impose la réalisation d’un bilan pré-opératoire avec une imagerie spécifique pour

préciser l’accessibilité endovasculaire, la morphologie et les mensurations aortiques en vue du

choix de l’endoprothèse la plus adaptée. En effet, l’étanchéité de ces réparations endovasculaires

de l’aorte thoracique est non seulement liée aux caractéristiques propres des endoprothèses, mais

également à sa taille par rapport au diamètre aortique et à la longueur d’aorte non pathologique

de part et d’autre de la lésion permettant l’implantation du dispositif endovasculaire (9). Ces

zones de largages ou collets doivent au minimum mesurer 20 mm pour assurer une fixation et une

étanchéité immédiates et durables. Pour les lésions situées à proximité des troncs supra-aortiques,

se pose alors le problème du devenir de l’artère sous-clavière gauche et de l’artère carotide

primitive gauche afin d’obtenir un collet suffisant pour permettre un traitement endovasculaire


4

efficace et sûr. La couverture de l’artère sous-clavière gauche est envisageable grâce aux

modifications de flux induisant un vol vertébral permettant sa revascularisation en distalité dans

la majorité des cas (10). La couverture de l’artère carotide primitive ou de l’artère sous-clavière

gauche en cas d’hypoplasie de l’artère vertébrale ipsilatérale nécessite alors une transposition

chirurgicale des troncs supra-aortiques préalable à la mise en place de l’endoprothèse (9). Ces

techniques hybrides ont permis d’élargir encore les indications de traitement endovasculaire des

lésions de l’aorte thoracique.

Néanmoins, ces principes de traitement endovasculaire ont également fait naître de

nouvelles complications telles que les endofuites, survenant parfois précocement ou plus

tardivement, plusieurs années après traitement endovasculaire, source de la plupart des

réinterventions nécessaires et faisant s’interroger sur la sécurité à long terme de ces nouveaux

traitements.

Les données actuellement disponibles dans la littérature sur la survie et les complications

à long-terme sont limitées, et la plupart des études réalisées ont un suivi inférieur à 2 ans (3,11).

Par ailleurs, si diverses pathologies de l’aorte thoracique sont accessibles à un traitement

endovasculaire, le pronostic semble conditionné par le terrain et le type de lésion aortique (12).

L’objectif de ce travail est d’évaluer après 6 ans de surveillance la survie et la survenue de

complications chez une cohorte de patients ayant bénéficié d’un traitement endovasculaire de

l’aorte thoracique en fonction de la pathologie traitée.


5

REFERENCES

1. Parodi JC, Palmaz JC, Barone HD. Transfemoral intraluminal graft implantation for

abdominal aortic aneurysms. Ann Vasc Surg. 1991 Nov;5(6):491–9.

2. Dake MD, Miller DC, Semba CP, Mitchell RS, Walker PJ, Liddell RP. Transluminal

placement of endovascular stent-grafts for the treatment of descending thoracic aortic aneurysms.

N Engl J Med. 1994 Dec 29;331(26):1729–34.

3. Attia C, Villard J, Boussel L, Farhat F, Robin J, Revel D, et al. Endovascular repair of

localized pathological lesions of the descending thoracic aorta: midterm results. Cardiovasc

Intervent Radiol. 2007 Aug;30(4):628–37.

4. Fairman RM, Criado F, Farber M, Kwolek C, Mehta M, White R, et al. Pivotal results of

the Medtronic Vascular Talent Thoracic Stent Graft System: the VALOR trial. J Vasc Surg. 2008

Sep;48(3):546–54.

5. Garzón G, Fernández-Velilla M, Martí M, Acitores I, Ybáñez F, Riera L. Endovascular

stent-graft treatment of thoracic aortic disease. Radiogr Rev Publ Radiol Soc N Am Inc. 2005

Oct;25 Suppl 1:S229–44.

6. Karimi A, Walker KL, Martin TD, Hess PJ, Klodell CT, Feezor RJ, et al. Midterm cost

and effectiveness of thoracic endovascular aortic repair versus open repair. Ann Thorac Surg.

2012 Feb;93(2):473–9.

7. Alric P, Canaud L, Branchereau P, Marty-Ane C. Traitement endovasculaire des

anévrismes de l’aorte thoracique descendante. 2012;43(148):1–20.


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8. Matsumura JS, Cambria RP, Dake MD, Moore RD, Svensson LG, Snyder S, et al.

International controlled clinical trial of thoracic endovascular aneurysm repair with the Zenith

TX2 endovascular graft: 1-year results. J Vasc Surg. 2008 Feb;47(2):247–58.

9. Rubin S, Baehrel B. Hybrid surgery of the thoracic aorta: theory and practical aspects. e-

mémoires de l’Académie Nationale de Chirurgie. 2010;87–94.

10. Kotelis D, Geisbüsch P, Hinz U, Hyhlik-Dürr A, von Tengg-Kobligk H, Allenberg JR, et

al. Short and midterm results after left subclavian artery coverage during endovascular repair of

the thoracic aorta. J Vasc Surg. 2009 Dec;50(6):1285–92.

11. Chaikof EL, Mutrie C, Kasirajan K, Milner R, Chen EP, Veeraswamy RK, et al.

Endovascular repair for diverse pathologies of the thoracic aorta: an initial decade of experience.

J Am Coll Surg. 2009 May;208(5):802–16; discussion 816–8.

12. Patterson B, Holt P, Nienaber C, Cambria R, Fairman R, Thompson M. Aortic pathology

determines midterm outcome after endovascular repair of the thoracic aorta: report from the

Medtronic Thoracic Endovascular Registry (MOTHER) database. Circulation. 2013 Jan

1;127(1):24–32.


7

1- RÉSUMÉ EN FRANÇAIS :

Objectif : Le traitement endovasculaire semble une alternative avantageuse dans la prise en

charge des lésions de l’aorte thoracique. Cependant l’évolution à long terme chez les patients

traités par endoprothèse est peu reportée dans la littérature. Cette étude rétrospective reporte

l’évolution à 6 ans après traitement endovasculaire de l’aorte thoracique.

Méthode : 74 patients ont bénéficié de traitement endovasculaire de l’aorte thoracique entre

1999 et 2007 : 13 dissections, 19 ruptures de l’isthme, 35 anévrismes, 6 pseudo-anévrismes et 1

ulcère. Le suivi moyen était de 5.9 ans, effectué annuellement par ARM ou angioscanner. La

mortalité globale et liée à la pathologie aortique, ainsi que les complications et réinterventions ont

été analysés.

Résultats : La mortalité globale (28/74 ; 37.8%) était plus élevée pour les anévrismes que

dans les autres groupes (57% (20/35) vs 20% (8/39); p<0.001). Les décès liés à l’aorte étaient de

14% (5/35) pour les anévrismes, nuls dans les autres groupes. Aucune complication tardive

n’était observée pour les ruptures de l’isthme, pseudo-anévrismes ou ulcères. La complication la

plus commune était l’endofuite ((21/74) ; 28.4 %), plus souvent type 1 et plus fréquente pour les

anévrismes que pour les autres groupes (48.6% vs 10% ; p<0.001. Une réintervention était

nécessaire chez 9 patients (10.8%), dont 7 anévrismes (9.5%). Le faux chenal était thrombosé

dans 53.8% des dissections (7/13), et diminuait de taille dans 38.5% (5/13). Le sac anévrismal


8

diminuait de taille chez seulement 17% des patients (6/35), alors qu’il augmentait chez 31%

(11/35).

Conclusion : L’évolution à long terme après TEVAR semble favorable pour les ruptures de

l’isthme aortique et les dissections de type B, avec un faible taux de mortalité globale et de

mortalité liée à la pathologie aortique.

En revanche, pour les anévrismes de l’aorte thoracique, la mortalité à long terme demeure

importante, malgré un faible taux de décès lié à la pathologie aortique elle-même, souvent

secondaire aux comorbidités plus importantes chez des patients athéromateux.


9

2- ABSTRACT

Objectives: Endovascular treatment of thoracic aortic lesions appears to be advantageous.

However, long-term outcomes remain poorly reported. This retrospective study reported 6-year

outcomes of thoracic endovascular aortic repair.

Methods: 74 patients underwent endovascular thoracic aorta treatments between 1999 and

2007; 13 had thoracic aortic dissections, 19 had traumatic aortic injuries, 35 had aneurysms, 6

had pseudoaneurysms, and 1 had a penetrating ulcer. The mean follow-up was 66 months after 30

perioperative days. Yearly follow-ups included computed tomography angiography or magnetic

resonance angiography. Patient demographics, mortality, complications, and reinterventions were

analyzed.

Results: The early 30-day mortality and the overall late mortality were respectively 9.5%

(7/74) and 37.8% (28/74). Late mortality was higher for aneurysms than other groups (20/35;

57% vs. 8/39; 20.5%; p=0.002). Aortic-related mortality occurred in 5/35 (14%) patients with

aneurysms, but not in other groups (p=0.02). No relationships among late complications were

found for traumatic aortic injuries. The most common complication was endoleak (21/74,

28.4%), which occurred more frequently with aneurysms than other disorders (18/35, 51.4% vs.

3/39, 7.7%; p<0.001). Endoleaks also occurred most frequently in aortic-related deaths (16/69 vs.

5/5; p=0.001). Type 1 endoleaks occurred significantly more often with aneurysms (13/35) than

with other disorders (p=0.004). Reintervention was required in 9 patients (12%); 8 with


10

atherosclerotic aneurysms (8/35; 23%). A false lumen thrombosed in 54% of dissections (7/13),

and shrank in 39% (5/13).

Conclusions: Long-term outcomes depended on aortic pathology. Aortic aneurysms were

the most complicated and caused the highest mortality, probably due to atherosclerotic disease

evolution. Patients with traumatic aortic injuries appeared to have the best long-term outcomes.


11

1. INTRODUCTION

Diseases of the thoracic aorta represent life-threatening conditions. Until recently, the only

effective treatment for these diseases was based on surgical graft replacement, involving

technically complex operations with high morbidity and mortality, particularly in patients with a

coexisting medical illness. Thoracic endovascular aortic repair (TEVAR) is revolutionizing the

management of thoracic aortic diseases by enabling minimally-invasive repair, even in high-risk

patients that are unfit for open surgery. Recently, several reports have demonstrated the short-

term safety and efficacy of endovascular stent-graft placement for thoracic aortic disease [1,2].

However, long-term data are limited; most studies had a mean of less than 2 years follow-up

[3,4]. Furthermore, endovascular stent-grafts have been used to treat various aortic diseases,

including thoracic aneurysm, dissections, and blunt traumatic injuries, which may lead to

different outcomes [5]. Therefore, it is important to determine whether the outcomes from

TEVAR are pathology-specific to enable the identification of subsets of patients that might

benefit most from endovascular treatment.

The purpose of this study was to evaluate pathology-specific, long-term outcomes and

complications in thoracic aortic lesions following endovascular treatment.


12

2. MATERIALS AND METHODS

We performed a retrospective review on data collected from 74 patients that underwent

TEVAR between April 1999 and December 2007 at a single center. Aortic lesions included 35

thoracic aortic aneurysms (33 degenerative and 2 mycotic aneurysms), 19 traumatic aortic

injuries, 13 dissections (5 Stanford type A, 6 Stanford type B, and 2 intramural hematomas [6]), 6

pseudo-aneurysms, and 1 penetrating ulcer.

TEVAR for acute lesions was indicated for traumatic ruptures of the isthmus, ruptured

aneurysms, or dissections, with malperfusion syndrome, uncontrollable hypertension, or

intractable pain. For chronic lesions, the indications were aneurysms > 50 mm of the descending

thoracic aorta, saccular aneurysms, penetrating aortic ulcer, and chronic dissection with aneurysm

dilatation of the descending aorta or compression of the true lumen.

2.1.Endovascular procedure

The endovascular procedure was performed in an angiographic suite (Philips Integris; Best;

the Netherlands) with patients under general anesthesia. Three preoperative vessel transpositions

(left subclavian artery or celiac trunk) were necessary to create an effective proximal or distal

neck length for maneuvering (minimum 20 mm).

Through a percutaneous access incision in the left brachial artery, a pigtail catheter was

placed to permit aortography before stent positioning. Through a femoral or iliac access incision,

a rigid guide wire was placed that extended up to the aortic root; over this, the endovascular stent

was inserted under fluoroscopic guidance. Either a Talent or Valiant device was used (Medtronic;


13

World Medical Manufacturing Corp., Sunrise, FL). The “free flow” part of the prosthesis was

positioned in front of the subclavian artery (isthmic aorta and aortic cross pathologies) or celiac

trunk (descending thoracic aorta pathologies). In absence of sufficient landing zone, subclavian

artery was covered by the “non free flow” part of the prosthesis, followed by occlusion of the

subclavian artery. However, because of vertebral steal, the distal subclavian artery remained

permeable and permitted to avoid vessel transposition most of the time.

The endoprothesis self-expanded to a diameter of 22 to 42 mm, which exceeded the

maximum diameter of the vessel necks by 10-20%. A final aortogram was performed to confirm

the correct positioning of the stent-graft and the exclusion of the lesion.

2.2.Clinical follow up

The primary outcome was overall survival. Kaplan-Meier curves for aortic-related death and

global death were calculated for the different groups of aortic pathologies. For patients with

multiple procedures, the first procedure was used to calculate survival. Cause of death was

determined by medical record, family interview, or autopsy report.

Aortic reinterventions were defined as the need to perform an additional procedure to treat a

complication or an ineffective initial TEVAR procedure. The reinterventions were classified as a

surgical, endovascular, or hybrid repair (aortic arch or visceral abdominal debranching with

endograft coverage).

Primary technical success, defined by the Society of Vascular Surgery reporting standards

[7], was based on immediate periprocedural events that occurred from the initiation of the

procedure through the first 24 h postoperatively.


14

2.3.Imaging evaluation

Before endovascular repair, computed tomography (CT) angiography was systematically

performed. We noted the maximum aneurysm diameter, dissection type, false lumen size,

proximal and distal extensions, and vessel neck diameters. After the procedure, CT angiography

or magnetic resonance angiography (MRA) was performed before discharge, then at 1, 3, 6, 12,

18, and 24 months, and then, at yearly follow-ups.

The main complication was endoleak, classified as types I through V [7]. Other

complications were peri-prosthetic aortic enlargement, migration of the endograft (≥10 mm

movement of the device inside the aorta), retrograde dissection, and aortoesophageal fistula.

Ancillary end points for dissections included the favorable evolution of a false lumen

(diameter either reduced by > 5 mm or stabilized) and thrombosis of a false lumen.

Aneurysm diameter evolution was also reported as an enlargement > 5 mm from baseline, a

regression > 5 mm, or stabilized.

2.4.Statistical analysis

Survival rates were compared between groups with different TEVAR indications with the

Log-rank (Mantel-Cox) Test.

Continuous variables are presented as the mean ± standard deviation with minimal and

maximal values (min-max). Categorical variables described in the tables are presented as a

percentage (raw number) and they were compared with a chi-square test.


15

A P value less than 0.05 was taken as the statistical significance threshold. All statistical

analysis was made with Intercooled Stata 9 (StataCorp LP, College Station, Texas, USA).


16

3. RESULTS

Seventy-four patients were followed after the TEVAR procedure, with a mean follow-up of

66 months (1.3-165), starting after 30 perioperative days. Two procedures were performed

between 1999 and 2001, 25 between 2002 and 2004, and 47 between 2005 and 2007.

The mean age of the entire study population was 60 ± 19 years, including 57 men and 17

women. In total, 8.1% (n=6) had diabetes, 17.6% (n=13) presented hypercholesterolemia, 37.8%

(n=28) had high blood pressure, and 51.3% (n=38) had a history of tobacco use. The patients

underwent 56.8% (n=42) elective and 43.2% (n=32) emergency procedures. Demographic and

clinical characteristics are summarized in Table 1, according to the indication subgroups.

Table 1. Demographic and clinical characteristics of patients

Variables Total (n=74) n (%)

Thoracic aortic dissections (n=13)

Thoracic aneurysms (n=35)

Traumatic aortic injuries (n=19)

Other aortic pathologies (n=7)

Age, y (mean±SD) 60 ± 18 60 ± 13 70 ± 12 39 ± 18 63 ± 15 Male/Female 57/17 9/4 26/9 16/3 6/1 Hypertension 28 (38) 9 (69) 15 (43) 1 (5) 3 (43) Obesity 4 (5) 2 (15) 0 2 (10.5) 0 Diabetes 6 (8) 3 (23) 3 (9) 0 0 Tobacco history 38 (51) 9 (69) 21 (60) 4 (21) 4 (57) Hypercholesterolemia 13 (18) 3 (23) 9 (26) 1 (5) 0 COPD 7 (9) 2 (15) 3 (9) 1 (5) 1 (14) Preoperative debranching

3 (4) 1 (8) 2 (6) 0 0

Procedure status Emergency 32 (43) 4 (31) 9 (26) 18 (95) 1 (14) Elective 42 (57) 9 (69) 26 (74) 1 (5) 6 (86) Date of procedure

1999-2001 2 (3) 0 0 1 (5) 1 (14) 2002-2004 23 (31) 4 (31) 8 (23) 6 (32) 5 (71) 2005-2007 49 (66) 9 (69) 27 (77) 12 (63) 1 (14)

COPD: Chronic Obstructive Pulmonary Disease


17

Primary technical success, as defined by the Society of Vascular Surgery reporting

standards7, was achieved in 71 procedures (96%); the other 3 patients (4%) were treated for

fissured aneurysms in emergency conditions and they developed endoleaks at the end of the

procedures. In 2 patients the suspected mechanism was a very high angulation of the thoracic

aorta in the landing zone. Regarding the third patient a device failure led to a type 3 endoleak.

There was no intra-operative mortality.

3.1.Perioperative mortality and adverse events

The overall 30-day mortality was 9.5% (7/74). The causes were 1 mesenteric ischemia, 1

aneurysm rupture, 1 cardiac rhythm disorder, 1 liver fracture, 1 splenic rupture, 1 myocardial

contusion, and 1 cerebral edema. Among these, 86% (6/7) occurred during emergency treatments.

There were 2 major perioperative adverse events: one was paraplegia and one was a

cerebrovascular accident.

3.2.Long-term mortality and adverse events

The global mortality was 37.8% (28/74). It was similar among patients that underwent

elective (35.7%; 15/42) and emergency procedures (40.6%; 13/32; p=0.849). Global mortality

was higher in the aneurysm group (57%; 20/35) than in other groups (21.6%; 8/39; p=0.002).

Patients with aneurysms also had the lowest long-term survival (45.9%) (Figure 1); the other

groups had survival rates of 76.9% for dissections, 84.2% for traumatic aortic injuries, and 71%

for other pathologies (p=0.0004).


18

Figure 1. Long-term survival in groups with different indications for TEVAR. (Top) aortic-

related overall survival; (Bottom) Long-term survival after the 30 peri-operative days.

Aortic-related mortality was 6.8% (5/74), including 3 aneurysm ruptures and 2 perioperative

deaths (1 endovascular reintervention and 1 surgical aortic replacement). The main causes of

non-aortic-related deaths were cardiac events, respiratory failure, and malignancy. Nevertheless,

the cause of death remained unclear for 5 patients. Mortality and major adverse events are

reported for patients grouped by the indication for TEVAR in Table 2.


19

Table 2. Mortality and major adverse events according to indications for TEVAR

Variables Total (n=74) % (n)

Thoracic aortic dissection (n=13) % (n)

Thoracic aneurysm (n=35) % (n)

Traumatic aortic injuries (n=19) % (n)

Other aortic pathologies (n=7) % (n)

Overall mortality 37.8 (28) 23.1 (3) 57.1 (20) 15.8 (3) 28.6 (2) Emergency 17.6 (13) 15.4 (2) 20 (7) 15.8 (3) 14.3 (1) Elective 20.3 (15) 7.7 (1) 37.1 (13) - 14.3 (1) Aortic related mortality 6.8 (5) - 14.3 (5) - - 30-day mortality 9.5 (7) 7.7 (1) 8.6 (3) 15.8 (3) - Emergency 8.1 (6) 77.7 (1) 5.7 (2) 15.8 (3) - Elective 1.3 (1) - 2.8 (1) - - Reinterventions 12.2 (9) 7.7 (1) 22.8 (8) - - Endovascular 4.0 (3) 7.7 (1) 5.7 (2) - - Surgical 4.0 (3) - 8.6 (3) - - Hybrid 4.0 (3) - 8.6 (3) - - Patients with endoleak 28.4 (21) 15.4 (2) 51.4 (18) 5.3 (1) - Number of endoleaks* 32 (24) 15.4 (2) 60 (21) 5.3 (1) - Type 1 62.5 (15/24) 100 (2/2) 62

(13/21) - -

Type 2 16.7 (4/24) - 19 (4/21) - - Type 3 12.5 (3/24) - 14 (3/21) - - Type 4 4.2 (1/24) - - 100 (1/1) - Unknown 4.2 (1/24) - 5 (1/21) - - Mean time from endoleak appearance (months)

21.2 (0-85) 23 (6-53) 22 (0-85) 0.5 -

Migration (> 10 mm) 1.3 (1) - 2.8 (1) - - Periprosthetic ectasia 6.7 (5) - 14.3 (5) - - Aortoesophageal fistula 1.3 (1) - 2.8 (1) - - Infection 1.3 (1) - 2.8 (1) - - Aneurysm size evolution Decrease > 5 mm - - 17.1 (6) - - Stable - - 51.4 (18) - - Increase > 5 mm - - 31.4 (11) - - Follow-up, months (range)

56 (0-165) 65 (0-110) 45 (1-130) 69 (0-165) 79 (6-128)

*Three patients had 2 endoleaks each; others had only 1 endoleak


20

Aortic reinterventions were required after 12.2% (9/74) of all TEVAR procedures. They

were performed with endovascular (n=3) (Figure 1), hybrid (n=3) (Figure 2), or open procedures

(n=3).

Figure 1: Type 1 endoleak after endovascular treatment of a descending thoracic aorta aneurysm

(top) successfully treated with a second endograft (bottom).


21

Figure 2: Type 2 endoleak (subclavian artery) treated by hybrid procedure with primitive carotid

artery and brachio-cephalic arterial trunk transposition, subclavian artery surgical exclusion

and second endograft insertion.

The indications for the reinterventions were mostly endoleaks, particularly type 1 (Table 3).

The mean period from TEVAR to the reintervention was 71 months (range: 8 – 113).

Table 3. Indications for aortic reintervention after TEVAR

Initial pathology Indication Procedure Period from primary TEVAR (months)

Dissection Mesenteric ischemia Endovascular 6 Mycotic aneurysm Aortoesophageal fistula Surgical 81 Degenerative aneurysm Type 1 endoleak Endovascular 112 Degenerative aneurysm Type 1 endoleak Endovascular 45 Degenerative aneurysm Type 1 endoleak Hybrid 44 Degenerative aneurysm Type 2 endoleak Surgical 8 Degenerative aneurysm Type 2 endoleak Hybrid 113 Degenerative aneurysm Type 3 endoleak Surgical 75

Degenerative aneurysm Migration and type 1 endoleak Hybrid 67


22

The most common complication was an endoleak (Figure 3 and 4). We observed 24

endoleaks in 21 patients (28.4%). Of these, 62.5% (15/24) were type 1, 16.7% (4/24) were type 2,

12.5% (3/24) were type 3, 4.2% (1/24) were type 4, and 4.2% (1/24) were unknown (suspected

endoleak with increased aneurysm size in absence of dye injection). Endoleaks occurred more

frequently in the aneurysm group (51.4%; 18/35) than in other groups (7.7%; 3/39; p<0.001).

They also occurred more frequently among aortic-related deaths (Figure 5) than among deaths

from other causes (5/5 vs. 16/69; p=0.001).

Figure 3: Type 1 endoleak after endovascular repair of thoracic aorta aneurysm. Rapid aneurism sac enlargement leading to aneurism rupture and death before any reintervention.


23

Figure 4: Images illustrate the detection of endoleaks. (a) Type 2 endoleak via left subclavian

artery, 7 years after TEVAR in a patient with an aneurysm. (b) Type 3 endoleak, due to an initial

endograft defect in a patient with an aneurysm.


24

Figure 5: Type 2 endoleak (intercostal artery) after endovascular treatment of thoracic aorta

aneurysm. Stability of aneurism size without reintervention since 2005.

3.3.Thoracic aortic aneurysms

Overall mortality in the aneurysm group was 57.1% (20/35), with 14.3% (5/35) aortic-related

deaths. The 30-day mortality rate was 8.6% (n=3).

Eighteen patients developed 21 endoleaks (3 patients presented 2 endoleaks each). Among

the endoleaks, 62% were type 1. One patient developed an endograft migration > 10 mm (Figure

6), and 1 patient developed an aortoesophageal fistula. Five patients (14.3%) developed aortic

enlargements at one end of the endograft.

At the initial assessment, the mean maximum aneurysm diameter was 62.4 ± 14.3 mm.

Among the 35 patients, the aneurysm size had increased by > 5 mm in 31.4% (n=11), decreased

by > 5 mm in 17.1% (n=6), and remained unchanged in 51.4% (n=18).


25

Figure 6: Images illustrate endograft migration one month after endovascular treatment of a

thoracic aorta aneurysm with type 1 endoleak then treated by hybrid procedure.

3.4.Thoracic dissections

Among the thoracic aortic dissections, 31% (4/13) were emergency procedures

(malperfusion syndrome with true lumen compression), and 69% (n=9) were elective procedures

(aneurismal evolution of a false lumen). The overall mortality was 23% (3/13), with no aortic-

related death.

Imaging studies showed that, among the 13 patients, the false lumen in the thoracic aorta

completely thrombosed in 54% (n=7) and shrank by > 5 mm in 39% (n=5) (Figure 7). Two

patients had type 1 endoleaks (15%), and two patients (15%) had intimo-medial erosions at the

distal endpoint of the prosthesis (Figure 8), with partial reperfusion of the false lumen, which

appeared 6 and 53 months after the TEVAR. Late outcomes in the dissection group are shown in

Table 4.


26

Figure 7:.Thrombosis and reduction of false lumen size in a patient with a dissection. CT images

show (top) parasagittal and (bottom) axial views of the false lumen at (left) one month and (right)

5 years after TEVAR.


27

Figure 8: Endovascular treatment of type B aortic dissection. Emergence of intimo-medial

erosion at the distal end-point of the prosthesis with partial reperfusion of the false lumen 6

months after TEVAR.

Table 4. Late outcomes for patients with dissections

Outcome Total (n=13)

Elective (n=9)

Emergency (n=4)

Overall mortality 23% (3) 11% (1) 50% (2) Aortic-related mortality 0 0 0 Intimo-medial erosion 15% (2) 22% (2) 0 False lumen thrombosis 54% (7) 55% (5) 50% (2) False lumen evolution Decrease > 5 mm 39% (5) 44% (4) 25% (1) Stable 46% (6) 44% (4) 50% (2) Increase > 5 mm 0 0 0 Unknown 15% (2) 11% (1) 25% (1)


28

3.5.Traumatic aortic injuries

The 19 patients that presented with traumatic ruptures of the thoracic aorta had experienced

road traffic accidents or suicide attempts and had sustained multiple injuries.

One primary type 4 endoleak sealed spontaneously before discharge (Figure 9). The 30-day

mortality rate was 15.8% (3/19): two patients died from hemorrhagic shock with a rupture of the

liver or spleen and one died from a myocardial contusion of the left ventricle. There was no

aortic-specific mortality.

The mean follow-up was 69 months (0-165), and all patients exhibited complete exclusion of

the aortic tear. There were no deaths, secondary endoleaks, or reinterventions.

Figure 9: Type 4 endoleak spontaneously resolutive three months after endovascular treatment of

an isthmic rupture.


29

3.6.Pseudo-aneurysms and penetrating ulcer

Six patients were treated for a pseudo-aneurysms of the thoracic aorta. The mean follow-up

was 79 months (6-128). Overall mortality was 33.3% (2/6), with no aortic-related death.

One patient was treated for a penetrating ulcer. The treatment was successful, with no

endoleaks or other complication after 19 months.


30

4. DISCUSSION

TEVAR is a recent, less invasive alternative to surgery for the treatment of several thoracic

aortic diseases. In the same period, around the half of the patients were treated by endovascular

therapy and the other half by open surgery. Although short-term outcomes of this procedure are

well-established, few studies have performed long-term follow-ups. Similar to previous works

[5,8], we found an overall survival of 62%, with high 5-year aortic-specific survival of 92%.

However, our subgroup analysis showed considerable differences in mortality among patients

with different indications. The 5-year global mortality rates ranged from 0% to 57%, and aortic-

related deaths ranged from 0% to 14%, depending on the indication. This finding illustrated that

outcomes after TEVAR are pathology-specific, as recently suggested in a study by Patterson [5].

4.1.Thoracic aortic aneurysm

Our long-term results revealed that the poorest survival occurred in patients with TAA (43%)

compared to those with other pathologies, as previously suggested [5,8]. However, the excess of

mortality in this group was principally caused by non-aortic related deaths, due to cardiac,

respiratory, and miscellaneous causes, as described by Patterson et al. [5]. This finding may be

explained by the fact that patients treated for TAA are often older individuals with significant

comorbidities.

Despite the well-known early effectiveness of TEVAR (global mortality from 8 to 10.3% vs.

2 to 3.6% with open repair) [9-11], the long-term efficacy of TEVAR continues to be debated. In

the present study, the overall mortality after TEVAR remained high; we found a 5-year rate of


31

57%, consistent with other studies [4,5,8,12]. In contrast, Karimi and colleagues did not find

differences in the 2-year survival rates between open repair and TEVAR (72% vs. 68%), and

TEVAR incurred a higher mean cumulative cost [9].

Furthermore, many patients developed complications after TEVAR. Endoleaks appeared to

be the most common complication; they affected about half of patients with TAA. Although the

rate of endoleaks in the present study was somewhat higher than that reported in other studies

(from 10.6% [2] to 47% [13]), the present study represented a longer mean follow-up. We

predominantly found type 1 endoleaks (62.5%). One third was caused by steep angulation or

enlargement of proximal or distal aorta. Thus we hypothesized that morphological degenerative

changes in the aorta may lead to angular modifications and enlargements at the ends of stent-

grafts, which may favor the appearance of endoleaks several months after TEVAR. However

technical aspect of endovascular treatment may also be considered: indeed we noted 2 initial

prosthesis malpositions and one prosthesis migration. The high frequency of endoleaks led to a

notable reintervention rate (23%).

The aneurismal morphological changes we observed included sac enlargements > 5 mm in

31% of patients, and reductions in only 17% of patients. Previous works showed a lower rate of

aneurysm growth (7.6% to 19%) [2,4,11]. This discrepancy might be explained by the longer

follow-up in our study (more than 45 months), and the higher rate of endoleaks, which can

sometimes occur several years after TEVAR. This hypothesis was supported by a previous

analysis in our hospital [3], which showed a reduction in the maximum aneurysm diameter in

69% of patients during a one-year follow-up period. Aneurysm enlargement continued after

endovascular repair in nearly one third of patients, which represented a persistent risk of rupture.

However, only 3 patients (4%) died from aneurysm ruptures, and TEVAR appeared to be


32

effective in preventing aortic-related death in patients with TAA. Despite the high risk of

endoleak and reinterventions, patients of greater age and disease severity may receive more

benefit with TEVAR, due to its lower short-term risk, compared to open repair. In contrast,

younger patients that are suitable for open surgical repair may benefit in the long run from a more

durable repair.

4.2.Thoracic dissection

It is well established that TEVAR offers significant advantages over open surgery for both

acute and chronic complicated dissections.

The overall mortality rate for aortic dissection (23%) found in this study was consistent with

rates reported previously (11% to 40%) [5,14-18], and with the early mortality rate (3% to 14%)

[5,15,18]. Overall and aortic-related mortality were higher in acute than in chronic dissections

(50% vs. 11% and 25% vs. 0%, respectively), as recently described [5].

After the initial perioperative phase, no aortic-related mortality occurred, which suggested

that endovascular therapy may prevent aortic rupture over a reasonable period. Despite the fact

that the perioperative mortality rate associated with endovascular repair was lower than that

associated with open surgery (11% vs. 29%, respectively), no differences were observed in long-

term survival rates (79.2% vs. 82.8%, respectively; p = 0.63) [16]. That finding suggested that

late mortality depends on comorbidities and age, rather than the aortic repair procedure.

Most studies have focused on Stanford type B aortic dissections. However, a new treatment

modality has emerged for selected patients with type A dissections that received a surgical

replacement of the ascending aorta combined with an endoluminal stent-graft repair for


33

descending thoracic aorta sites. We included both Stanford type B and Stanford type A

dissections in patients that previously received thoracic ascending aorta surgery. After proximal

aortic repair for an acute aortic dissection type A, patients with true lumen compression and

malperfusion syndrome of the downstream aorta should receive TEVAR early to alleviate or even

prevent ischemic injury [19]. We found no differences in mortality rates (20% vs. 33%) or

complications among patients with type A or type B dissections.

Theoretically, a stent-graft placement over the intimal entry tear should restore normal blood

flow in the true lumen and induce thrombosis and shrinkage of the false lumen. We observed

progressive aortic remodeling with complete thrombosis of the false lumen in 54% and a

decrease in the false lumen > 5 mm in 39% of patients after 5 years, as previously described

[10,15]. However, other works observed more than 80% false lumen thromboses after 2 or 3

years [14,20].

We observed no enlargements in false lumens. Thus, we suggest that TEVAR might have

merely delayed the natural course of the disease and aneurysm formation. However, we could not

confirm a link between favorable aortic remodeling and favorable long-term outcomes. Similarly,

the INSTEAD trial compared optimal medical treatment to medical and endovascular treatments

in patients with chronic type B dissections. They could not demonstrate any difference in all-

cause deaths or aortic-related deaths between the two groups, despite favorable aortic remodeling

with endovascular treatment (false lumen was thrombosed in 91% with endovascular treatment

vs. 19% with optimal medical treatment) [17].

We observed distal erosion of the intimo-medial flap in 2 patients (15%) treated for chronic

dissection after a follow-up period of 6 to 53 months. This finding was consistent with a previous

study by Yang and colleagues [14], who found distal intimo-medial erosion in 19% of acute


34

dissections and 36% of chronic dissections. The erosion appeared more frequently in patients

with chronic dissection than in those with acute dissection, probably due to the fragility of the

aortic wall in those with chronic dissections. Indeed, during the chronic phase, the adventitia and

intimal flaps become rigid and fibrotic, with reduced capacity for prominent remodeling.

4.3.Traumatic aortic injuries

Recent investigations showed that traumatic rupture of the thoracic aorta occurs in 21% of

vehicle crashes with adult fatalities [21]. In patients that survive the initial period, surgical repair

of these aortic lesions has been the gold standard for many decades. However, this surgical

approach was associated with significant early mortality (21%) and morbidity rates (nearly 10%

paraplegia) [22]. Recently, the stent graft device was introduced as a less invasive alternative

treatment for thoracic aortic injuries, and it was associated with reduced mortality and morbidity

rates [23]. The early mortality rate was 16%, averaged over several studies (2.4% to 24%) [24-

25]. The stent procedure did not cause any aortic-related deaths; instead, patients died from other

injuries (brain injury, spleen rupture …). In the present study, we found that the long-term

survival after TEVAR was higher in this group than in the aneurysm and dissection groups (84%

vs. 43% and 77%, respectively), consistent with a previous study by Shah et al. [8]. This finding

was not surprising, because these patients with traumatic aortic ruptures were often younger and

had less comorbidities than patients in other groups.

Despite the many benefits shown in short- and mid-term outcomes, extended long-term

outcomes (more than 10 years after TEVAR) remain a major issue in relatively young patients

with long life expectancies. Young patients have high potential for future degenerative changes,


35

due to age-related increases in the thoracic aorta diameter (1.5 mm per decade). To our

knowledge, no report has analyzed outcomes more than 10 years after TEVAR, and the mean age

of patients that undergo this procedure is 39 +/- 18 years old. Thus, most patients are expected to

live for more than 30 years after a TEVAR. The correct sizing of the stent-graft appeared to be a

crucial factor. It should be oversized to avoid migration, but not too large, to avoid collapse[24].

4.4.Pseudo-aneurysms and penetrating ulcers

Endovascular treatment for pseudo-aneurysms or penetrating ulcer appeared to be a safe,

effective procedure with no associated aortic-related deaths or complications. However, our study

only included a few patients in these groups; thus, the numbers may be insufficient to generalize

our findings.

4.5.Limitations

The primary limitation of this study was that it only included only 74 patients, with small

subgroup populations. This small group size makes it difficult to generalize our findings,

particularly for the dissection, aortic ulcer, and pseudo-aneurysm groups. However, this single

center experience showed differences in global and aortic mortality between aneurysms and other

subgroups similar to those reported in other, larger studies [5].


36

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Cite this article as: Dufour C, Gamondes D, Mansuy A, Robin J, Boussel L, Douek P. Pathology-specific late outcome after endovascular repair of thoracic aorta: asingle-centre experience. Eur J Cardiothorac Surg 2015; doi:10.1093/ejcts/ezv054.

Pathology-specific late outcome after endovascular repair ofthoracic aorta: a single-centre experience

Clémence Dufoura,*, Delphine Gamondesa, Adeline Mansuya, Jacques Robinb, Loïc Boussela and

Philippe Doueka

a Department of Interventional Radiology and Cardio-vascular and Thoracic Diagnostic Imaging, Louis Pradel University Hospital, Bron, Franceb Department of Cardio-vascular Surgery, Louis Pradel University Hospital, Bron, France

* Corresponding author. Department of Interventional Radiology and Cardio-vascular and Thoracic Diagnostic Imaging, Louis Pradel University Hospital, 59Boulevard Pinel, 69677 Bron Cedex, France. Tel: +33-6-63387493; fax: +33-4-72357363; e-mail: [email protected] (C. Dufour).

Received 11 November 2014; received in revised form 22 December 2014; accepted 29 December 2014

Abstract

OBJECTIVES: Endovascular treatment of thoracic aortic lesions appears to be advantageous. However, long-term outcomes remain poorlyreported. This retrospective study reported 6-year outcomes of thoracic endovascular aortic repair.

METHODS: A total of 74 patients underwent endovascular thoracic aorta treatments between 1999 and 2007; 13 had thoracic aortic dis-sections, 19 had traumatic aortic injuries, 35 had aneurysms, 6 had pseudoaneurysms and 1 had a penetrating ulcer. The mean follow-upwas 66 months after 30 perioperative days. Yearly follow-ups included computed tomography angiography or magnetic resonance angi-ography. Patient demographics, mortality, complications and reinterventions were analysed.

RESULTS: The early 30-day mortality and the overall late mortality were 9.5 (7/74) and 37.8% (28/74), respectively. Late mortality washigher in patients with aneurysms than in the other groups (20/35; 57% vs 8/39; 20.5%; P = 0.002). Aortic-related mortality occurred in 5/35(14%) patients with aneurysms, but not in other groups (P = 0.02). No relationships among late complications were found for traumaticaortic injuries. The most common complication was an endoleak (21/74, 28.4%), which occurred more frequently with aneurysms thanother disorders (18/35, 51.4% vs 3/39, 7.7%; P < 0.001). Endoleaks also occurred most frequently in aortic-related deaths (16/69 vs 5/5;P = 0.001). Type 1 endoleaks occurred significantly more often with aneurysms (13/35) than with other disorders (P = 0.004). Reinterventionwas required in 9 patients (12%); 8 with atherosclerotic aneurysms (8/35; 23%). A false lumen was thrombosed in 54% of dissections (7/13),and shrank in 39% (5/13).

CONCLUSIONS: Long-term outcomes depended on aortic pathology. Aortic aneurysms were the most complicated and caused the highestmortality, probably due to atherosclerotic disease evolution. Patients with traumatic aortic injuries appeared to have the best long-term out-comes.

Keywords: Thoracic aorta • Endovascular repair • Endoleak

INTRODUCTION

Diseases of the thoracic aorta represent life-threatening condi-tions. Until recently, the only effective treatment for these diseaseswas based on surgical graft replacement, involving technicallycomplex operations with high morbidity and mortality, particular-ly in patients with a coexisting medical illness. Thoracic endovas-cular aortic repair (TEVAR) is revolutionizing the management ofthoracic aortic diseases by enabling minimally invasive repair,even in high-risk patients that are unfit for open surgery. Recently,several reports have demonstrated the short-term safety and effi-cacy of endovascular stent graft placement for thoracic aorticdisease [1, 2]. However, long-term data are limited; most studieshad a mean of less than 2-years follow-up [3, 4]. Furthermore,endovascular stent grafts have been used to treat various aorticdiseases, including thoracic aneurysm, dissections and blunt

traumatic injuries, which may lead to different outcomes [5].Therefore, it is important to determine whether the outcomes fromTEVAR are pathology-specific to enable the identification of subsetsof patients that might benefit most from endovascular treatment.The purpose of this study was to evaluate pathology-specific,

long-term outcomes and complications in thoracic aortic lesionsfollowing endovascular treatment.

MATERIALS ANDMETHODS

We performed a retrospective review on data collected from74 patients that underwent TEVAR between April 1999 andDecember 2007 at a single centre. Aortic lesions included 35 thor-acic aortic aneurysms (33 degenerative and 2 mycotic aneurysms),19 traumatic aortic injuries, 13 dissections (5 Stanford type A, 6

© The Author 2015. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved.

AORTICSU

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European Journal of Cardio-Thoracic Surgery (2015) 1–9 ORIGINAL ARTICLEdoi:10.1093/ejcts/ezv054

European Journal of Cardio-Thoracic Surgery Advance Access published February 26, 2015


Stanford type B and 2 intramural haematomas [6]), 6 pseudo-aneurysms and 1 penetrating ulcer.

TEVAR for acute lesions was indicated for traumatic ruptures ofthe isthmus, ruptured aneurysms or dissections, with malperfusionsyndrome, uncontrollable hypertension or intractable pain. Forchronic lesions, the indications were aneurysms >50 mm of thedescending thoracic aorta, saccular aneurysms, penetrating aorticulcer and chronic dissection with aneurysm dilatation of the des-cending aorta or compression of the true lumen.

Endovascular procedure

The endovascular procedure was performed in an angiographicsuite (Philips Integris; Best; The Netherlands) with patients undergeneral anaesthesia. Three preoperative vessel transpositions(left subclavian artery or celiac trunk) were necessary to createan effective proximal or distal neck length for manoeuvering(minimum 20 mm).

Through a percutaneous access incision in the left brachialartery, a pigtail catheter was placed to permit aortography beforestent positioning. Through a femoral or iliac access incision, a rigidguide wire was placed that extended up to the aortic root; overthis, the endovascular stent was inserted under fluoroscopic guid-ance. Either a Talent or Valiant device was used (Medtronic; WorldMedical Manufacturing Corp., Sunrise, FL, USA). The ‘free flow’part of the prosthesis was positioned in front of the subclavianartery (isthmic aorta and aortic cross pathologies) or celiac trunk(descending thoracic aorta pathologies). In the absence of suffi-cient landing zone, subclavian artery was covered by the “non-free flow” part of the prosthesis, followed by occlusion of thesubclavian artery. However, because of vertebral steal, the distalsubclavian artery remained permeable and enabled one to avoidvessel transposition most of the time.

The endoprosthesis self-expanded to a diameter of 22–42 mm,which exceeded the maximum diameter of the vessel necks by10–20%. A final aortogram was performed to confirm the correctpositioning of the stent graft and the exclusion of the lesion.

Clinical follow-up

The primary outcome was overall survival. Kaplan–Meier curvesfor aortic-related death and global death were calculated for thedifferent groups of aortic pathologies. For patients with multipleprocedures, the first procedure was used to calculate survival.Cause of death was determined by medical record, family inter-view or autopsy report.

Aortic reinterventions were defined as the need to perform anadditional procedure to treat a complication or an ineffectiveinitial TEVAR procedure. The reinterventions were classified as asurgical, endovascular or hybrid repair (aortic arch or visceral ab-dominal debranching with endograft coverage).

Primary technical success, defined by the Society of VascularSurgery reporting standards [7], was based on immediate peripro-cedural events that occurred from the initiation of the procedurethrough to the first 24 h postoperatively.

Imaging evaluation

Before endovascular repair, computed tomography (CT) angiog-raphy was systematically performed. We noted the maximum an-eurysm diameter, dissection type, false lumen size, proximal and

distal extensions and vessel neck diameters. After the procedure,CT angiography or magnetic resonance angiography (MRA) wasperformed before discharge, then at 1, 3, 6, 12, 18 and 24 months,and then, at yearly follow-ups.The main complication were endoleaks, classified as Types I–V

[7]. Other complications were periprosthetic aortic enlargement,migration of the endograft (≥10 mm movement of the deviceinside the aorta), retrograde dissection and aorto-oesophagealfistula. Ancillary end-points for dissections included the favourableevolution of a false lumen (diameter either reduced by >5 mm orstabilized) and thrombosis of a false lumen. Aneurysm diameterevolution was also reported as an enlargement of >5 mm frombaseline, a regression of >5 mm or stabilized.

Statistical analysis

Survival rates were compared between groups with differentTEVAR indications with the log-rank (Mantel–Cox) test. Continuousvariables are presented as the mean ± standard deviation withminimal and maximal values (min–max). Categorical variablesdescribed in the tables are presented as a percentage (rawnumber) and they were compared with a χ2 test. A P-value of<0.05 was taken as the statistical significance threshold. All statis-tical analysis was made with Intercooled Stata 9 (StataCorp LP,College Station, TX, USA).

RESULTS

Seventy-four patients were followed after the TEVAR procedure,with a mean follow-up of 66 months (1.3–165), starting after 30perioperative days. Two procedures were performed between1999 and 2001, 25 between 2002 and 2004 and 47 between 2005and 2007.The mean age of the entire study population was 60 ± 19 years,

including 57 men and 17 women. In total, 8.1% (n = 6) had dia-betes, 17.6% (n = 13) presented hypercholesterolaemia, 37.8%(n = 28) had high blood pressure and 51.3% (n = 38) had a historyof tobacco use. The patients underwent 56.8% (n = 42) electiveand 43.2% (n = 32) emergency procedures. Demographic and clin-ical characteristics are summarized in Table 1, according to the in-dication subgroups.Primary technical success, as defined by the Society of Vascular

Surgery reporting standards [7], was achieved in 71 procedures(96%); the other 3 patients (4%) were treated for fissured aneur-ysms in emergency conditions and they developed endoleaks atthe end of the procedures. In 2 patients, the suspected mechan-ism was a very high angulation of the thoracic aorta in the landingzone. Regarding the third patient, a device failure led to a type 3endoleak. There was no intraoperative mortality.

Perioperative mortality and adverse events

The overall 30-day mortality was 9.5% (7/74). The causes were1 mesenteric ischaemia, 1 aneurysm rupture, 1 cardiac rhythmdisorder, 1 liver fracture, 1 splenic rupture, 1 myocardial contu-sion and 1 cerebral oedema. Among these, 86% (6/7) occurredduring emergency treatments. There were 2 major perioperativeadverse events: 1 was paraplegia and 1 was a cerebrovascularaccident.

C. Dufour et al. / European Journal of Cardio-Thoracic Surgery2


Long-term mortality and adverse events

The global mortality was 37.8% (28/74). It was similar amongpatients that underwent elective (35.7%; 15/42) and emergencyprocedures (40.6%; 13/32; P = 0.849). Global mortality was higherin the aneurysm group (57%; 20/35) than in other groups (21.6%;8/39; P = 0.002). Patients with aneurysms also had the lowest long-term survival (45.9%) (Fig. 1); the other groups had survival rates of76.9% for dissections, 84.2% for traumatic aortic injuries and 71%for other pathologies (P = 0.0004).

Aortic-related mortality was 6.8% (5/74), including 3 aneurysmruptures and 2 perioperative deaths (1 endovascular reinterventionand 1 surgical aortic replacement). The main causes of non-aortic-related deaths were cardiac events, respiratory failure and malig-nancy. Nevertheless, the cause of death remained unclear for5 patients. Mortality and major adverse events are reported forpatients grouped by the indication for TEVAR in Table 2.

Aortic reinterventions were required after 12.2% (9/74) of allTEVAR procedures. They were performed with endovascular(n = 3), hybrid (n = 3) or open procedures (n = 3). The indicationsfor the reinterventions were mostly endoleaks, particularly type 1(Table 3). The mean period from TEVAR to the reintervention was71 months (range: 8–113).

The most common complication was an endoleak (Fig. 2).We observed 24 endoleaks in 21 patients (28.4%). Of these, 62.5%(15/24) were type 1, 16.7% (4/24) were type 2, 12.5% (3/24) weretype 3, 4.2% (1/24) were type 4 and 4.2% (1/24) were unknown (sus-pected endoleak with increased aneurysm size in the absence ofdye injection). Endoleaks occurred more frequently in the aneurysmgroup (51.4%; 18/35) than in other groups (7.7%; 3/39; P < 0.001).They also occurred more frequently among aortic-related deathsthan among deaths from other causes (5/5 vs 16/69; P = 0.001).

Thoracic aortic aneurysms

Overall mortality in the aneurysm group was 57.1% (20/35), with14.3% (5/35) aortic-related deaths. The 30-day mortality rate was8.6% (n = 3).

Eighteen patients developed 21 endoleaks (3 patients presented2 endoleaks each). Among the endoleaks, 62% were type 1. Onepatient developed an endograft migration >10 mm, and 1 patientdeveloped an aorto-oesophageal fistula. Five patients (14.3%) de-veloped aortic enlargements at one end of the endograft.At the initial assessment, the mean maximum aneurysm diam-

eter was 62.4 ± 14.3 mm. Among the 35 patients, the aneurysmsize had increased by >5 mm in 31.4% (n = 11), decreased by >5 mmin 17.1% (n = 6) and remained unchanged in 51.4% (n = 18).

Table 1: Demographic and clinical characteristics of patients

Variables Total (n = 74)n (%)

Thoracic aorticdissections (n = 13)

Thoracic aneurysms(n = 35)

Traumatic aorticinjuries (n = 19)

Other aorticpathologies (n = 7)

Age [years (mean ± SD)] 60 ± 18 60 ± 13 70 ± 12 39 ± 18 63 ± 15Male/female 57/17 9/4 26/9 16/3 6/1Hypertension 28 (38) 9 (69) 15 (43) 1 (5) 3 (43)Obesity 4 (5) 2 (15) 0 2 (10.5) 0Diabetes 6 (8) 3 (23) 3 (9) 0 0Tobacco history 38 (51) 9 (69) 21 (60) 4 (21) 4 (57)Hypercholesterolaemia 13 (18) 3 (23) 9 (26) 1 (5) 0COPD 7 (9) 2 (15) 3 (9) 1 (5) 1 (14)Preoperative debranching 3 (4) 1 (8) 2 (6) 0 0Procedure statusEmergency 32 (43) 4 (31) 9 (26) 18 (95) 1 (14)Elective 42 (57) 9 (69) 26 (74) 1 (5) 6 (86)

Date of procedure1999–2001 2 (3) 0 0 1 (5) 1 (14)2002–2004 23 (31) 4 (31) 8 (23) 6 (32) 5 (71)2005–2007 49 (66) 9 (69) 27 (77) 12 (63) 1 (14)

COPD: chronic obstructive pulmonary disease.

Figure 1: Long-term survival in groups with different indications for TEVAR.Aortic-related overall survival (A); long-term survival after the 30 perioperativedays (B). TEVAR: thoracic endovascular aortic repair.

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Thoracic dissections

Among the thoracic aortic dissections, 31% (4/13) were emer-gency procedures (malperfusion syndrome with true lumen com-pression) and 69% (n = 9) were elective procedures (aneurysmalevolution of a false lumen). The overall mortality was 23% (3/13),with no aortic-related death.

Imaging studies showed that, among the 13 patients, the falselumen in the thoracic aorta completely was thrombosed in 54%(n = 7) and shrank by >5 mm in 39% (n = 5) (Fig. 3). Two patientshad type 1 endoleaks (15%), and 2 patients (15%) had intimo-

medial erosions at the distal end-point of the prosthesis, withpartial reperfusion of the false lumen, which appeared 6 and 53months after the TEVAR. Late outcomes in the dissection groupare given in Table 4.

Traumatic aortic injuries

The 19 patients that presented with traumatic ruptures of thethoracic aorta had experienced road traffic accidents or suicideattempts, and had sustained multiple injuries.

Table 2: Mortality and major adverse events according to indications for TEVAR

Variables Total (n = 74)% (n)

Thoracic aorticdissection(n = 13) % (n)

Thoracicaneurysm(n = 35) % (n)

Traumatic aorticinjuries (n = 19) % (n)

Other aorticpathologies(n = 7) % (n)

Overall mortality 37.8 (28) 23.1 (3) 57.1 (20) 15.8 (3) 28.6 (2)Emergency 17.6 (13) 15.4 (2) 20 (7) 15.8 (3) 14.3 (1)Elective 20.3 (15) 7.7 (1) 37.1 (13) — 14.3 (1)

Aortic-related mortality 6.8 (5) — 14.3 (5) — —

30-day mortality 9.5 (7) 7.7 (1) 8.6 (3) 15.8 (3) —

Emergency 8.1 (6) 77.7 (1) 5.7 (2) 15.8 (3) —

Elective 1.3 (1) — 2.8 (1) — —

Reinterventions 12.2 (9) 7.7 (1) 22.8 (8) — —

Endovascular 4.0 (3) 7.7 (1) 5.7 (2) — —

Surgical 4.0 (3) — 8.6 (3) — —

Hybrid 4.0 (3) — 8.6 (3) — —

Patients with endoleak 28.4 (21) 15.4 (2) 51.4 (18) 5.3 (1) —

Number of endoleaksa 32 (24) 15.4 (2) 60 (21) 5.3 (1) —

Type 1 62.5 (15/24) 100 (2/2) 62 (13/21) — —

Type 2 16.7 (4/24) — 19 (4/21) — —

Type 3 12.5 (3/24) — 14 (3/21) — —

Type 4 4.2 (1/24) — — 100 (1/1) —

Unknown 4.2 (1/24) — 5 (1/21) — —

Mean time from endoleak appearance (months) 21.2 (0–85) 23 (6–53) 22 (0–85) 0.5 —

Migration (>10 mm) 1.3 (1) — 2.8 (1) — —

Periprosthetic ectasia 6.7 (5) — 14.3 (5) — —

Aorto-oesophageal fistula 1.3 (1) — 2.8 (1) — —

Infection 1.3 (1) — 2.8 (1) — —

Aneurysm size evolutionDecrease >5 mm — — 17.1 (6) — —

Stable — — 51.4 (18) — —

Increase >5 mm — — 31.4 (11) — —

Follow-up, months (range) 56 (0–165) 65 (0–110) 45 (1–130) 69 (0–165) 79 (6–128)

TEVAR: thoracic endovascular aortic repair.aThree patients had two endoleaks each; others had only one endoleak.

Table 3: Indications for aortic reintervention after TEVAR

Initial pathology Indication Procedure Period from primaryTEVAR (months)

Dissection Mesenteric ischaemia Endovascular 6Mycotic aneurysm Aorto-oesophageal fistula Surgical 81Degenerative aneurysm Type 1 endoleak Endovascular 112Degenerative aneurysm Type 1 endoleak Endovascular 45Degenerative aneurysm Type 1 endoleak Hybrid 44Degenerative aneurysm Type 2 endoleak Surgical 8Degenerative aneurysm Type 2 endoleak Hybrid 113Degenerative aneurysm Type 3 endoleak Surgical 75Degenerative aneurysm Migration and type 1 endoleak Hybrid 67



One primary type 4 endoleak sealed spontaneously before dis-charge. The 30-day mortality rate was 15.8% (3/19): 2 patientsdied from haemorrhagic shock with a rupture of the liver orspleen and 1 died from a myocardial contusion of the left ven-tricle. There was no aortic-specific mortality.

The mean follow-up was 69 months (0–165), and all patientsexhibited complete exclusion of the aortic tear. There were nodeaths, secondary endoleaks or reinterventions.

Pseudo-aneurysms and penetrating ulcer

Six patients were treated for a pseudo-aneurysm of the thoracicaorta. The mean follow-up was 79 months (6–128). Overall mor-tality was 33.3% (2/6), with no aortic-related death.

One patient was treated for a penetrating ulcer. The treatmentwas successful, with no endoleaks or other complication after19 months.

DISCUSSION

TEVAR is a recent, less invasive alternative to surgery for the treat-ment of several thoracic aortic diseases. In the same period,around half of the patients were treated by endovascular therapyand the other half by open surgery. Although short-term out-comes of this procedure are well established, few studies have

performed the long-term follow-ups. Similar to previous works[5, 8], we found an overall survival of 62%, with high 5-year aortic-specific survival of 92%. However, our subgroup analysis showedconsiderable differences in mortality among patients with differ-ent indications. The 5-year global mortality rates ranged from 0 to57%, and aortic-related deaths ranged from 0 to 14%, dependingon the indication. This finding illustrated that outcomes afterTEVAR are pathology-specific, as recently suggested in a study byPatterson et al. [5].

Thoracic aortic aneurysm

Our long-term results revealed that the poorest survival occurredin patients with thoracic aortic aneurysm (TAA) (43%) comparedwith those with other pathologies, as previously suggested [5, 8].However, the excess of mortality in this group was principallycaused by non-aortic-related deaths, due to cardiac, respiratoryand miscellaneous causes, as described by Patterson et al. [5]. Thisfinding may be explained by the fact that patients treated for TAAare often older individuals with significant comorbidities.Despite the well-known early effectiveness of TEVAR (global

mortality from 8 to 10.3% vs 2 to 3.6% with open repair) [9–11],the long-term efficacy of TEVAR continues to be debated. In thepresent study, the overall mortality after TEVAR remained high; wefound a 5-year rate of 57%, consistent with other studies [4, 5,8, 12]. In contrast, Karimi et al. [9] did not find differences in the

Figure 2: Images illustrate the detection of endoleaks. (A) Type 2 endoleak via left subclavian artery, 7 years after TEVAR in a patient with an aneurysm. (B) Type 3endoleak, due to an initial endograft defect in a patient with an aneurysm. TEVAR: thoracic endovascular aortic repair.

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2-year survival rates between open repair and TEVAR (72 vs 68%),and TEVAR incurred a higher mean cumulative cost.

Furthermore, many patients developed complications afterTEVAR. Endoleaks appeared to be the most common complica-tion; they affected about half of patients with TAA. Although therate of endoleaks in the present study was somewhat higher than

that reported in other studies (from 10.6 [2] to 47% [13]), thepresent study represented a longer mean follow-up. We predom-inantly found type 1 endoleaks (62.5%). One-third was caused bysteep angulation or enlargement of proximal or distal aorta. Thus,we hypothesized that morphological degenerative changes in theaorta may lead to angular modifications and enlargements at the

Figure 3: Thrombosis and reduction of false lumen size in a patient with a dissection. CT images show (top) parasagittal and (bottom) axial views of the false lumen at(left) 1 month and (right) 5 years after TEVAR. TEVAR: thoracic endovascular aortic repair; CT: computed tomography.



ends of stent grafts, which may favour the development of endo-leaks several months after TEVAR. However, the technical aspectof endovascular treatment may also be considered: indeed, wenoted 2 initial prosthesis malpositions and one prosthesis migra-tion. The high frequency of endoleaks led to a notable reinterven-tion rate (23%).

The aneurysmal morphological changes we observed includedsac enlargements >5 mm in 31% of patients, and reductions inonly 17% of patients. Previous works showed a lower rate of an-eurysm growth (7.6–19%) [2, 4, 11]. This discrepancy might beexplained by the longer follow-up in our study (more than 45months), and the higher rate of endoleaks, which can sometimesoccur several years after TEVAR. This hypothesis was supported bya previous analysis in our hospital [3], which showed a reductionin the maximum aneurysm diameter in 69% of patients during a1-year follow-up period. Aneurysm enlargement continued afterendovascular repair in nearly one-third of patients, which repre-sented a persistent risk of rupture. However, only 3 patients (4%)died from aneurysm ruptures, and TEVAR appeared to be effectivein preventing aortic-related death in patients with TAA. Despitethe high risk of endoleak and reinterventions, patients of greaterage and disease severity may receive more benefit with TEVAR,due to its lower short-term risk, compared with open repair. Incontrast, younger patients that are suitable for open surgical repairmay benefit in the long run from a more durable repair.

Thoracic dissection

It is well established that TEVAR offers significant advantages overopen surgery for both acute and chronic complicated dissections.

The overall mortality rate for aortic dissection (23%) found inthis study was consistent with rates reported previously (11–40%)[5, 14–18], and with the early mortality rate (3–14%) [5, 15, 18].Overall and aortic-related mortality were higher in acute than inchronic dissections (50 vs 11% and 25 vs 0%, respectively), as re-cently described [5].

After the initial perioperative phase, no aortic-related mortalityoccurred, which suggested that endovascular therapy may preventaortic rupture over a reasonable period. Despite the fact that theperioperative mortality rate associated with endovascular repairwas lower than that associated with open surgery (11 vs 29%, re-spectively), no differences were observed in long-term survivalrates (79.2 vs 82.8%, respectively; P = 0.63) [16]. That finding sug-gested that late mortality depends on comorbidities and age,rather than the aortic repair procedure.

Most studies have focused on Stanford type B aortic dissections.However, a new treatment modality has emerged for selectedpatients with type A dissections that received a surgical replace-ment of the ascending aorta combined with an endoluminalstent-graft repair for descending thoracic aorta sites. We includedboth Stanford type B and Stanford type A dissections in patientsthat previously received thoracic ascending aorta surgery. Afterproximal aortic repair for an acute aortic dissection type A,patients with true lumen compression and malperfusion syn-drome of the downstream aorta should receive TEVAR early to al-leviate or even prevent ischaemic injury [19]. We found nodifferences in mortality rates (20 vs 33%) or complications amongpatients with type A or type B dissections.Theoretically, a stent-graft placement over the intimal entry tear

should restore normal blood flow in the true lumen, and inducethrombosis and shrinkage of the false lumen. We observed pro-gressive aortic remodelling with complete thrombosis of the falselumen in 54% and a decrease in the false lumen >5 mm in 39% ofpatients after 5 years, as previously described [10, 15]. However,other works observed >80% false lumen thromboses after 2 or 3years [14, 20].We observed no enlargements in false lumens. Thus, we suggest

that TEVAR might have merely delayed the natural course of thedisease and aneurysm formation. However, we could not confirma link between favourable aortic remodelling and favourablelong-term outcomes. Similarly, The INvestigation of STEnt grafts inaortic Dissection trial compared optimal medical treatment withmedical and endovascular treatments in patients with chronictype B dissections. They could not demonstrate any difference inall-cause deaths or aortic-related deaths between the two groups,despite favourable aortic remodelling with endovascular treat-ment (false lumen was thrombosed in 91% with endovasculartreatment vs 19% with optimal medical treatment) [17].We observed distal erosion of the intimo-medial flap in 2 pa-

tients (15%) treated for chronic dissection after a follow-up periodof 6–53 months. This finding was consistent with a previous studyby Yang et al. [14], who found distal intimo-medial erosion in 19%of acute dissections and 36% of chronic dissections. The erosionappeared more frequently in patients with chronic dissection thanin those with acute dissection, probably due to the fragility of theaortic wall in those with chronic dissections. Indeed, during thechronic phase, the adventitia and intimal flaps become rigid andfibrotic, with reduced capacity for prominent remodelling.

Traumatic aortic injuries

Recent investigations showed that traumatic rupture of the thor-acic aorta occurs in 21% of vehicle crashes with adult fatalities [21].In patients that survive the initial period, surgical repair of theseaortic lesions has been the gold standard for many decades.However, this surgical approach was associated with significantearly mortality (21%) and morbidity rates (nearly 10% paraplegia)[22]. Recently, the stent graft device was introduced as a less inva-sive alternative treatment for thoracic aortic injuries, and it wasassociated with reduced mortality and morbidity rates [23]. Theearly mortality rate was 16%, averaged over several studies (2.4–24%) [24, 25]. The stent procedure did not cause any aortic-relateddeaths; instead, patients died from other injuries (such as braininjury and spleen rupture). In the present study, we found that thelong-term survival after TEVAR was higher in this group than in theaneurysm and dissection groups (84 vs 43 and 77%, respectively),

Table 4: Late outcomes for patients with dissections

Outcome Total(n = 13)

Elective(n = 9)

Emergency(n = 4)

Overall mortality 23% (3) 11% (1) 50% (2)Aortic-related mortality 0 0 0Intimo-medial erosion 15% (2) 22% (2) 0False lumen thrombosis 54% (7) 55% (5) 50% (2)False lumen evolutionDecrease >5 mm 39% (5) 44% (4) 25% (1)Stable 46% (6) 44% (4) 50% (2)Increase >5 mm 0 0 0Unknown 15% (2) 11% (1) 25% (1)

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consistent with a previous study by Shah et al. [8]. This finding wasnot surprising, because these patients with traumatic aortic rup-tures were often younger and had less comorbidities than patientsin other groups.

Despite the many benefits shown in short- and mid-term out-comes, extended long-term outcomes (more than 10 years afterTEVAR) remain a major issue in relatively young patients with longlife expectancies. Young patients have high potential for future de-generative changes, due to age-related increases in the thoracicaorta diameter (1.5 mm per decade). To our knowledge, no reporthas analysed outcomes more than 10 years after TEVAR, and themean age of patients who undergo this procedure is 39 ± 18 yearsold. Thus, most patients are expected to live for more than 30years after a TEVAR. The correct sizing of the stent-graft appearedto be a crucial factor. It should be oversized to avoid migration,but not too large, to avoid collapse [24].

Pseudo-aneurysms and penetrating ulcers

Endovascular treatment for pseudo-aneurysms or penetratingulcer appeared to be a safe, effective procedure with no asso-ciated aortic-related deaths or complications. However, our studyonly included a few patients in these groups; thus, the numbersmay be insufficient to generalize our findings.

Limitations

The primary limitation of this study was that it only included 74patients, with small subgroup populations. This small group sizemakes it difficult to generalize our findings, particularly for the dis-section, aortic ulcer and pseudo-aneurysm groups. However, thissingle-centre experience showed differences in global and aorticmortality between aneurysms and other subgroups similar to thosereported in other, larger studies [5].

The present study showed that long-term outcomes of TEVARdepended on the aortic pathology and associated comorbidities.Long-term aortic-related survival after TEVAR was high and rein-tervention was infrequent in patients with thoracic dissections,traumatic aortic injuries and pseudo-aneurysms. Conversely, inpatients with TAA, the overall long-term mortality was relativelyhigh. This high late mortality rate suggested that patients with TAAmay represent a subset in which underlying comorbidities pose agreater risk of death than the aortic disease alone. In addition, wesuggest that the high rates of endoleaks and reinterventions forpatients with TAA were probably secondary to underlying aorticmorphological changes related to atherosclerosis.

Conflict of interest: none declared.

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DUFOUR Clémence Traitement endovasculaire des pathologies aigües et chroniques de l’aorte thoracique : évaluation après 6 ans de surveillance. 10 Figures, 4 tableaux, 63 pages Thèse de Médecine: Lyon 2015 n°

ABSTRACT : Objectives: Endovascular treatment of thoracic aortic lesions appears to be advantageous. However, long-term outcomes remain poorly reported. This retrospective study reported 6-year outcomes of thoracic endovascular aortic repair. Methods: 74 patients underwent endovascular thoracic aorta treatments between 1999 and 2007; 13 had thoracic aortic dissections, 19 had traumatic aortic injuries, 35 had aneurysms, 6 had pseudoaneurysms, and 1 had a penetrating ulcer. The mean follow-up was 66 months after 30 perioperative days. Yearly follow-ups included computed tomography angiography or magnetic resonance angiography. Patient demographics, mortality, complications, and reinterventions were analyzed. Results: The early 30-day mortality and the overall late mortality were respectively 9.5% (7/74) and 37.8% (28/74). Late mortality was higher for aneurysms than other groups (20/35; 57% vs. 8/39; 20.5%; p=0.002). Aortic-related mortality occurred in 5/35 (14%) patients with aneurysms, but not in other groups (p=0.02). No relationships among late complications were found for traumatic aortic injuries. The most common complication was endoleak (21/74, 28.4%), which occurred more frequently with aneurysms than other disorders (18/35, 51.4% vs. 3/39, 7.7%; p<0.001). Endoleaks also occurred most frequently in aortic-related deaths (16/69 vs. 5/5; p=0.001). Type 1 endoleaks occurred significantly more often with aneurysms (13/35) than with other disorders (p=0.004). Reintervention was required in 9 patients (12%); 8 with atherosclerotic aneurysms (8/35; 23%). A false lumen thrombosed in 54% of dissections (7/13), and shrank in 39% (5/13). Conclusions: Long-term outcomes depended on aortic pathology. Aortic aneurysms were the most complicated and caused the highest mortality, probably due to atherosclerotic disease evolution. Patients with traumatic aortic injuries appeared to have the best long-term outcomes.

MOTS-CLES : Endovascular repair, thoracic aorta, aneurism, type B dissection, traumatic aortic injury

JURY :

- Président : Monsieur le Professeur Philippe Douek - Membres : Monsieur le Professeur Didier Revel

Monsieur le Professeur Jean-Pierre Pracros Monsieur le Professeur Laurent Guibaud Monsieur le Professeur Loïc Boussel Monsieur le Docteur Jacques Robin

Date de soutenance : le 26 Mai 2015

Adresse de l’auteur : 107 cours Gambetta 69003 Lyon clé[email protected]


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